期刊
PLOS ONE
卷 11, 期 6, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0156442
关键词
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资金
- program Investissements d'Avenir [ANR- JCJC SVSE 5 2011, Labex CelTisPhyBio ANR-10-LBX-0038 ANR-10-IDEX-0001-02 PSL]
- Cells-in-Motion Cluster of Excellence, University of Munster, Germany [EXC 1003 - CiM]
- Institut Thematique Multi-organismes Cancer - Plan Cancer
- Ecole Doctorale Frontieres du Vivant (FdV) - Programme Bettencourt
- Fondation pour la Recherche Medicale (FRM) [DGE20111123020]
- Cancerople-IdF [2012-2-EML-04-IC-1]
- InCA (Cancer National Institute) [2011-1-LABEL-IC-4]
- SiRIC@ CNRS-Institut Curie [INCa-DGOS- 4654]
- PICT-IBiSA@ CNRS-Institut Curie [INCa-DGOS- 4654]
- Nikon Imaging Center@ CNRS-Institut Curie [INCa-DGOS- 4654]
The mechanical properties of tumors and the tumor environment provide important information for the progression and characterization of cancer. Tumors are surrounded by an extracellular matrix (ECM) dominated by collagen I. The geometrical and mechanical properties of the ECM play an important role for the initial step in the formation of metastasis, presented by the migration of malignant cells towards new settlements as well as the vascular and lymphatic system. The extent of this cell invasion into the ECM is a key medical marker for cancer prognosis. In vivo studies reveal an increased stiffness and different architecture of tumor tissue when compared to its healthy counterparts. The observed parallel collagen organization on the tumor border and radial arrangement at the invasion zone has raised the question about the mechanisms organizing these structures. Here we study the effect of contractile forces originated from model tumor spheroids embedded in a biomimetic collagen I matrix. We show that contractile forces act immediately after seeding and deform the ECM, thus leading to tensile radial forces within the matrix. Relaxation of this tension via cutting the collagen does reduce invasion, showing a mechanical relation between the tensile state of the ECM and invasion. In turn, these results suggest that tensile forces in the ECM facilitate invasion. Furthermore, simultaneous contraction of the ECM and tumor growth leads to the condensation and reorientation of the collagen at the spheroid's surface. We propose a tension-based model to explain the collagen organization and the onset of invasion by forces originating from the tumor.
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